Greater relative weight is associated with higher blood pressure, but the reasons are unknown. The inability of current technology to induce sustained weight loss among overweight persons precludes experimental tests of whether this association is causal. We evaluated the degree to which the covariation between body mass index (BMI; kg/m2) and blood pressure (BP) among women is due to pleiotropic genetic factors, environmental factors, or phenotypic causation. The sample included 75 monozygotic (MZ) and 39 dizygotic (DZ) pairs of adult female twins. "BP" was calculated as the unit-weighted mean of systolic and diastolic. Data were analyzed through structural equation modeling. A model was specified stipulating that additive genetic effects (A) and unique environmental effects (E) each contributed to the covariance between BMI and BP, thus allowing for both pleiotropic and unique environmental influences on the covariance between BMI and BP. Dropping the pleiotropic influences significantly worsened the model (chi 2 = 4.62, df = 1, P = .032), suggesting significant pleiotropic effects. Dropping the environmental influences on the cross-phenotype covariance did not significantly worsen the model (chi 2 = 1.42, df = 1, P = .233). This indicates no significant effect of the environment on the covariance between BMI and BP. Finally, a model of phenotypic causation in which BMI directly influenced BP was fitted. This model provided the best single parameter explanation of the BP-BMI covariation. These data suggest that, among women, regardless of the source of variation, changes in BMI should lead to long-standing changes in BP.